Abstract
The acceptance of oestradiol signalling through receptors found in the cell membrane, as well as, the nucleus, has provided for a re-examination of the timing and location of the actions of oestradiol on neural circuits mediating sexual receptivity (lordosis). Oestradiol membrane signalling involves the transactivation of metabotrophic glutamate receptors (mGluRs) that transduce steroid information through protein kinase C signalling cascades producing rapid activation of lordosis-regulating circuits. It has been known for some time that oestradiol initially produces an inhibition of the medial preoptic nucleus. We have demonstrated that underlying this inhibition is oestradiol acting in the arcuate nucleus to induce β-endorphin release, which inhibits the medial preoptic nucleus through a μ-opioid receptor mechanism. This transient inhibition is relieved by either subsequent progesterone treatment or longer exposure to higher doses of oestradiol to facilitate lordosis behaviour. We review recent findings about oestradiol membrane signalling inducing dendritic spine formation in the arcuate nucleus that is critical for oestradiol induction of sexual receptivity. Moreover, we discuss the evidence that, in addition to oestrogen receptor α, several other putative membrane oestrogen receptors facilitate lordosis behaviour through regulation of the arcuate nucleus. These include the GRP30 and the STX activated Gq-mER. Finally, we report on the importance of GABA acting at GABAB receptors for oestradiol membrane signalling that regulates lordosis circuit activation and sexual receptivity.